5-Azacytidine Reactivates E-cadherin via Promoter Demethylation and Induces Autophagy in Colorectal Cancer Cells | ||
| Egyptian Journal of Chemistry | ||
| Articles in Press, Accepted Manuscript, Available Online from 29 October 2025 | ||
| Document Type: Original Article | ||
| DOI: 10.21608/ejchem.2025.418977.12264 | ||
| Authors | ||
| Muhamed El Nobey* 1; Salim El-Hamidy2; Abdulkader Omar2; Khalid AI-Ghamdi1 | ||
| 1Department of Biological Sciences, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia | ||
| 21Department of Biological Sciences, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia 2Princess Doctor Najla Bint Saud Al Saud Distinguished Research Centre for Biotechnology, King Abdulaziz University, Jeddah, Saudi Arabia | ||
| Abstract | ||
| Colorectal cancer (CRC) is a severe neoplasm that is associated with high mortality rates. Aberrant epigenetic alterations are associated with several stages of tumor growth. The FDA has approved 5-Azacytidine (5-aza) for the treatment of specific types of cancers, including leukemia and MDS. Previous studies have demonstrated that E-cadherin1 (CDH1) expression is suppressed in CRC. However, the regulatory mechanisms underlying CDH1 suppression remain unclear. This investigation focused on examining whether 5-aza has a significant effect on CRC treatment using the human LS513 cell line. MTT test was used to evaluate the LS513 cell viability following 5-aza treatment; cell proliferation along with autophagy were assessed using flow cytometry; CDH1 expression was analyzed by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blotting, while methylation-specific PCR (MSP-PCR) was used to investigate the degree of methylation in the CDH1 promoter region. These Findings indicate that 5-aza reduced the viability of LS513 cells in a concentration-dependent manner (P < 0.05). 5-aza treatment arrested the cell cycle at the G2/M phase, triggered autophagy, and upregulated CDH1 expression following deactivation of the hypermethylated CDH1 promoter. | ||
| Keywords | ||
| Colorectal cancer; DNA methylation; 5-Azacytidine; CDH1 | ||
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